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Human hepatocellular carcinoma (HCC) is associated with high mortality rates, being the third most common cause of cancer death worldwide. Although estrogens have been implicated in HCC, their potential role in development and/or progression of this malignancy remains unclear. In this study we investigated mRNA and protein expression of aromatase (Aro) and amphiregulin (AREG) in relation to estrogen receptors (ERs), in HepG2, Huh7, and HA22T human malignant liver cell lines, using RT-PCR and Western blot analyses. Aro expression was significantly higher (∼13-fold, P= 0.003) in HepG2 cells than in Huh7 cells, while no Aro expression could be detected in HA22T cells. Interestingly, the patterns of AREG expression were consistently associated with those of Aro, with ∼3-fold and ∼8-fold higher levels being seen in HepG2 cells than in Huh7 cells ( P= 0.002) and HA22T cells ( P= 0.0014), respectively. Using a specific set of primers, ERα46 is the only ER variant expressed in all cell lines, while the wild-type ERα66 could not be detected. Western blot analysis revealed a corresponding figure. This evidence suggests that AREG expression may be upregulated by estrogens in human HCC and that locally elevated aromatase activity also may increase malignant cell proliferation through AREG signaling. [ABSTRACT FROM AUTHOR]

In this study, we investigated androgen metabolism in two different human prostate cancer cell lines, the androgen-responsive LNCaP cells and the nonresponsive PC3 cells. Following 24-h and 72-h incubation with either testosterone (T) or androstenedione (Ad) used as precursor, divergent patterns and rates of androgen metabolism were observed. Given the recent interest in the multiple uses of embryonic and adult stem cells for basic and applied research, we compared the expression of three presumptive stem cell markers (Oct-4, SUZ-12, and Cripto-1), along with connexin 43 (Cx43), Cx32, and androgen receptor (AR), used as cell differentiation gene markers. In anchorage-independent cell growth conditions, the expression levels of candidate markers of cancer stem cells initially increased (days 2–4) but drastically fell thereafter (day 6) in both cell lines. Results of immunocytochemical assay (ICA) largely confirmed those obtained by RT-PCR. Interestingly, both symmetrical and asymmetrical cell divisions were revealed in PC3 cells using Oct-4 immunostaining. Our data suggest that both androgen-responsive and androgen-nonresponsive prostate tumor cell lines contain a presumptive cancer stem cell population that can be identified using a panel of selected gene markers, including Oct-4, SUZ-12, and Cripto-1. [ABSTRACT FROM AUTHOR]

A new classification based on gene expression profiling or immunohistochemical (IHC) characteristics may replace current histopathological classifications and predict better clinical outcomes. We used IHC markers to classify incident cases ascertained by the Palermo Breast Cancer Registry (2002–2004) into four subtypes: luminal-A (ER+ or PgR+ and HER2/neu−); luminal-B (ER+ or PgR+, HER2/neu+); basal-like (ER−, PgR−, HER2/neu−); and HER2+/ER− (HER2/neu+, ER−, PgR−). We evaluated HER2/neu, ER and PgR in 1300/1985 (65%) cases. The most common IHC-subtype was luminal-A (68%), whereas luminal-B, basal-like, and HER2+/ER− accounted for 14%, 13%, and 5%, respectively. IHC-subtypes were not associated with tumor size, geographic location within the province, or menopause, but differed by NPI ( P < 0.0001), grading ( P < 0.0001), lymph-node involvement ( P= 0.04), metastases ( P= 0.04), and TNM stage ( P= 0.04). Endocrine therapy was administered to 81% of 519 postmenopausal, luminal-A, and luminal-B cases and to 32% of 114 postmenopausal, basal-like, and HER2+/ER− cases. [ABSTRACT FROM AUTHOR]

The theory that viruses play a role in human cancers is now supported by scientific evidence. In fact, around 12% of human cancers, a leading cause of morbidity and mortality in some regions, are attributed to viral infections. However, the molecular mechanism remains complex to decipher. In recent decades, the uncovering of cellular miRNAs, with their invaluable potential as diagnostic and prognostic biomarkers, has increased the number of studies being conducted regarding human cancer diagnosis. Viruses develop clever mechanisms to succeed in the maintenance of the viral life cycle, and some viruses, especially herpesviruses, encode for miRNA, v-miRNAs. Through this viral miRNA, the viruses are able to manipulate cellular and viral gene expression, driving carcinogenesis and escaping the host innate or adaptive immune system. In this review, we have discussed the main viral miRNAs and virally influenced cellular pathways, and their capability to drive carcinogenesis. [ABSTRACT FROM AUTHOR]